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ACTH deficiency, hyperprolactinemia and benign intracranial hypertension. A case report
1Department of Medicine, University of Tromsø, Norway.
Insights
A young woman developed adrenal insufficiency and intracranial hypertension postpartum. Prompt cortisone therapy led to full recovery, suggesting a possible autoimmune cause for her pituitary dysfunction.
Area of Science:
- Endocrinology
- Neuroendocrinology
- Reproductive Medicine
Background:
- Postpartum endocrine dysfunction can manifest with diverse symptoms.
- Adrenocorticotropic hormone (ACTH) deficiency can lead to adrenal insufficiency.
- Benign intracranial hypertension (BIH) presents with neurological symptoms.
Observation:
- A 26-year-old female presented with symptoms of adrenal insufficiency and amenorrhea one year postpartum.
- She developed critical illness with hypotension during an infection, followed by symptoms of intracranial hypertension.
- Endocrine evaluation revealed secondary adrenocortical failure and moderately elevated prolactin (PRL).
Findings:
- Pituitary ACTH and cortisol levels failed to respond to corticotropin-releasing hormone (CRH), indicating a pituitary lesion.
- Other pituitary hormone reserves (TSH, GH, LH, FSH) and a CT scan were normal.
- Cortisone substitution therapy resulted in immediate clinical recovery and restoration of menstruation and fertility within a year.
Implications:
- This case highlights a potential autoimmune etiology for isolated ACTH deficiency precipitated in the puerperium.
- Early diagnosis and management of secondary adrenal insufficiency are crucial for patient outcomes.
- The interplay between postpartum hormonal changes and pituitary function warrants further investigation.
Abstract:
A 26-year-old female with ACTH deficiency, hyperprolactinemia and benign intracranial hypertension is reported. Her symptoms of adrenocortical insufficiency and persistent amenorrhea appeared after her last child birth one year previously. During an infectious disease she became critically ill with hypotension and was treated with iv penicillin. A bacterial infection was, however, not diagnosed. After 4 days she developed symptoms and signs of intracranial hypertension. She improved gradually within 10 days without specific therapy against the intracranial pressure. Endocrine investigation disclosed a secondary adrenocortical failure. The lesion appeared to be located in the pituitary gland since plasma ACTH and cortisol did not respond to CRH. A moderately elevated serum PRL was found, whereas the pituitary reserves of TSH, GH, LH and FSH were normal, as was a computed tomographic scan of the pituitary gland. The patient was given cortisone substitution therapy and recovered immediately. Within the following year she regained normal menstruations and became pregnant. A possible autoimmune etiology of her isolated ACTH deficiency precipitated in the puerperium is discussed.